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KCC2 Activation Reverses Neurophysiological and Behavioral Deficits in Female Rett Mice.

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    Activating KCC2 (SLC12A5) with OV350 improved motor coordination, sociability, and reduced seizures in Rett syndrome mouse models. This suggests KCC2 activation may treat neurodevelopmental disorders.

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    Area of Science:

    • Neuroscience
    • Genetics
    • Pharmacology

    Background:

    • Rett syndrome is an X-linked neurodevelopmental disorder caused by MeCP2 gene mutations.
    • Pathophysiology involves impaired synaptic inhibition due to altered GABAergic currents.
    • Neuronal chloride extrusion via SLC12A5 (KCC2) is crucial for inhibitory GABAergic currents.

    Purpose of the Study:

    • To investigate if KCC2 activation can ameliorate Rett syndrome phenotypes in female MeCP2+/- mice.
    • To assess the therapeutic potential of OV350, a direct KCC2 activator.

    Main Methods:

    • Utilized female MeCP2+/- mice as a model for Rett syndrome.
    • Administered OV350, a direct KCC2 activator.
    • Performed EEG recordings and behavioral assessments (motor coordination, sociability, spatial memory).
    • Analyzed KCC2 phosphorylation levels.

    Main Results:

    • OV350 treatment rapidly reduced EEG power and epileptic discharge severity.
    • Significant improvements were observed in motor coordination, sociability, and spatial memory.
    • MeCP2+/- mice exhibited deficits in KCC2 phosphorylation, which were reversed by OV350.

    Conclusions:

    • KCC2 activation effectively ameliorated key Rett syndrome phenotypes in a mouse model.
    • Targeting KCC2 represents a promising therapeutic strategy for Rett syndrome.
    • KCC2 activation may offer benefits for other neurodevelopmental disorders with similar pathophysiology.